Non‐Surgical Periodontal Therapy Reduces Saliva Adipokine and Matrix Metalloproteinase Levels in Periodontitis

Abstract

Adipokines may contribute to the breakdown of periodontal tissue in periodontitis by stimulating the expression of proinflammatory cytokines and MMPs.

Salivary Colony Stimulating Factor‐1 and Interleukin‐34 in Periodontal Disease

“…CSF‐1 shows similar trends to MMP‐8. The present findings support previous reports of the potential of whole saliva to mirror periodontal inflammation through the presence of molecules associated with periodontal pathogenesis 6‐8,10 …”

“…In patients with periodontitis, however, CSF‐1 and MMP‐8 stayed high after treatment despite improvement in clinical periodontal parameters. Published works by others on salivary MMP‐8 after treatment of periodontitis in patients differ depending on the time point for follow‐up 8 , 33 , 34 . MMP‐8 levels in gingival crevicular fluid (GCF) during wound healing after surgery were found increased at 2 and 4 weeks compared with baseline and decreased between 2 and 12 weeks 35 .…”

“…Saliva has potential to reflect local and systemic status through presence of inflammatory and immune components related to pathogenesis and diagnosis 4 , 5 . Salivary interleukin (IL)‐1β and matrix metalloproteinase (MMP)‐8 increase in periodontitis, and levels restore after treatment 6–8 . This is in accordance with their functions in periodontal pathogenesis where IL‐1β is the primary signaling cytokine in periodontal lesions and a potent recruiter of neutrophils 9 .…”

Salivary, gingival crevicular fluid and serum levels of ghrelin and chemerin in patients with periodontitis and overweight

“…Immunomodulatory effects of chemerin might be both inflammatory and anti‐inflammatory. The potential inflammatory function of chemerin in periodontitis might be underlined by the fact that the levels of chemerin in gingival crevicular fluid and saliva decreased after periodontal therapy. In synovial fibroblasts, chemerin increased expression of toll‐like receptor 4 and of the chemokine (C‐C motif) ligand 2 .…”

Role of the Hypoxia-Inducible Factor in Periodontal Inflammation

“…Researchers often investigate the levels of such biological markers in the periodontium in atempts to gauge the severity of periodontal disease and monitor periodontal treatment outcomes [33]. Recent studies reported that a hypoxic environment may upregulate proinlammatory cytokines and MMPs' expression from host cells during periodontal disease [34]. The idea was that hypoxia further encourages lipopolysaccharide (LPS)-induced TNF-α, interleukin-1β, and interleukin 6 (IL-6) expressions via LPS toll-like receptor (TLR) interaction that, in turn, activates the nuclear factor kappa B (NF-κB) pathway in human PDL cells upon exposure to the aforementioned Gram-negative bacterial surface component [35][36][37].…”